Pub Date : 2024-11-05DOI: 10.1016/j.phrs.2024.107489
Xu Tan , Yu Wang , Lei Long , Hongdan Chen , Langfan Qu , Xiaohui Cao , Huijuan Li , Zelin Chen , Shenglin Luo , Chunmeng Shi
Cancer immunotherapy remains a low immune response rate in clinic because of dominant immunosuppressive tumor microenvironment (TME) and lack of effective drug to specifically remodel the TME. In this work, we introduced a tumor-seeking human serum albumin (HSA) based delivery platform by covalently conjugating with a tumor-targeting near-infrared (NIR) photosensitizer (IR-DBI) and non-covalently loading of immune modulator Resiquimod (R848). HSA exhibited tumor-preferential accumulation after covalent conjugation with IR-DBI. Meanwhile, HSA restricted the rotation of IR-DBI, narrowed the HOMO-LUMO energy gap, significantly enhanced fluorescent intensity and dual-modal phototherapy (PTT/PDT). The enhanced phototherapeutic effect further induced robust ICD effect. More importantly, non-covalent loading of R848 could be released from HSA at tumor sites by laser irradiation-induced heat. The in-situ release of R848 in TME efficiently promoted the maturation of DC cells and repolarized M2 macrophages to M1 macrophages. Consequently, robust photo-induced antitumor immunity was triggered in the different mice models bearing primary and distant tumors or lung metastasis, which was further enhanced by combining with CTLA-4 blockade therapy. Taken together, this work may present a versatile albumin composite which exhibits tumor-preferential accumulation and imaging-guided PDT/PTT/immunotherapy.
{"title":"A theranostic photosensitizer-conjugated albumin co-loading with resiquimod for cancer-targeted imaging and robust photo-immunotherapy","authors":"Xu Tan , Yu Wang , Lei Long , Hongdan Chen , Langfan Qu , Xiaohui Cao , Huijuan Li , Zelin Chen , Shenglin Luo , Chunmeng Shi","doi":"10.1016/j.phrs.2024.107489","DOIUrl":"10.1016/j.phrs.2024.107489","url":null,"abstract":"<div><div>Cancer immunotherapy remains a low immune response rate in clinic because of dominant immunosuppressive tumor microenvironment (TME) and lack of effective drug to specifically remodel the TME. In this work, we introduced a tumor-seeking human serum albumin (HSA) based delivery platform by covalently conjugating with a tumor-targeting near-infrared (NIR) photosensitizer (IR-DBI) and non-covalently loading of immune modulator Resiquimod (R848). HSA exhibited tumor-preferential accumulation after covalent conjugation with IR-DBI. Meanwhile, HSA restricted the rotation of IR-DBI, narrowed the HOMO-LUMO energy gap, significantly enhanced fluorescent intensity and dual-modal phototherapy (PTT/PDT). The enhanced phototherapeutic effect further induced robust ICD effect. More importantly, non-covalent loading of R848 could be released from HSA at tumor sites by laser irradiation-induced heat. The in-situ release of R848 in TME efficiently promoted the maturation of DC cells and repolarized M2 macrophages to M1 macrophages. Consequently, robust photo-induced antitumor immunity was triggered in the different mice models bearing primary and distant tumors or lung metastasis, which was further enhanced by combining with CTLA-4 blockade therapy. Taken together, this work may present a versatile albumin composite which exhibits tumor-preferential accumulation and imaging-guided PDT/PTT/immunotherapy.</div></div>","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"210 ","pages":"Article 107489"},"PeriodicalIF":9.1,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-05DOI: 10.1016/j.phrs.2024.107490
Shiwen Ma , Fei Xie , Xiaohu Wen , Yao Mawulikplimi Adzavon , Ruping Zhao , Jinyi Zhao , Han Li , Yanqi Li , Jingtao Liu , Chen Liu , Yang Yi , Pengxiang Zhao , Boqing Wang , Wei Zhao , Xuemei Ma
The emergence of sorafenib resistance has become a predominant impediment and formidable dilemma in the therapeutic approach for hepatocellular carcinoma (HCC). Although the approval of next-generation drugs as alternatives to sorafenib is a significant development, the concurrent use of inhibitors that target additional key molecular pathways remains an effective strategy to mitigate the acquisition of resistance. Here, we identified Glutathione S-Transferase Alpha 1 (GSTA1) as a critical modulator of sorafenib resistance (SR) in hepatocellular carcinoma (HCC) based on our findings from experiments conducted on recurrent liver cancer tissues, xenograft mouse models, organoids, and sorafenib-resistant cells. Elevated GSTA1 levels are strongly associated with adverse clinical prognoses. The knockout of GSTA1 reinstates sorafenib sensitivity, whereas its overexpression attenuates drug efficacy. Mechanistically, GSTA1 enhances the accumulation of lipid peroxides and suppresses ferroptosis by exerting its peroxidase function to regulate the SR. Notably, the upregulation of GSTA1 expression is mediated by the transcription factor CTNNB1 (β-catenin), resulting in the formation of a cytoplasmic complex between GSTA1 and CTNNB1. This complex facilitates the nuclear translocation of CTNNB1, establishing a positive feedback loop. The combined use of GSTA1 and CTNNB1 inhibitors demonstrated synergistic anti-tumour effects through the induction of ferroptosis both in vitro and in vivo. Our findings reveal a novel regulatory role of the GSTA1/CTNNB1 axis in ferroptosis, suggesting that targeting GSTA1 and CTNNB1 could be a promising strategy to circumvent sorafenib resistance in HCC.
{"title":"GSTA1/CTNNB1 axis facilitates sorafenib resistance via suppressing ferroptosis in hepatocellular carcinoma","authors":"Shiwen Ma , Fei Xie , Xiaohu Wen , Yao Mawulikplimi Adzavon , Ruping Zhao , Jinyi Zhao , Han Li , Yanqi Li , Jingtao Liu , Chen Liu , Yang Yi , Pengxiang Zhao , Boqing Wang , Wei Zhao , Xuemei Ma","doi":"10.1016/j.phrs.2024.107490","DOIUrl":"10.1016/j.phrs.2024.107490","url":null,"abstract":"<div><div>The emergence of sorafenib resistance has become a predominant impediment and formidable dilemma in the therapeutic approach for hepatocellular carcinoma (HCC). Although the approval of next-generation drugs as alternatives to sorafenib is a significant development, the concurrent use of inhibitors that target additional key molecular pathways remains an effective strategy to mitigate the acquisition of resistance. Here, we identified Glutathione S-Transferase Alpha 1 (GSTA1) as a critical modulator of sorafenib resistance (SR) in hepatocellular carcinoma (HCC) based on our findings from experiments conducted on recurrent liver cancer tissues, xenograft mouse models, organoids, and sorafenib-resistant cells. Elevated GSTA1 levels are strongly associated with adverse clinical prognoses. The knockout of GSTA1 reinstates sorafenib sensitivity, whereas its overexpression attenuates drug efficacy. Mechanistically, GSTA1 enhances the accumulation of lipid peroxides and suppresses ferroptosis by exerting its peroxidase function to regulate the SR. Notably, the upregulation of GSTA1 expression is mediated by the transcription factor CTNNB1 (β-catenin), resulting in the formation of a cytoplasmic complex between GSTA1 and CTNNB1. This complex facilitates the nuclear translocation of CTNNB1, establishing a positive feedback loop. The combined use of GSTA1 and CTNNB1 inhibitors demonstrated synergistic anti-tumour effects through the induction of ferroptosis both in vitro and in vivo. Our findings reveal a novel regulatory role of the GSTA1/CTNNB1 axis in ferroptosis, suggesting that targeting GSTA1 and CTNNB1 could be a promising strategy to circumvent sorafenib resistance in HCC.</div></div>","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"210 ","pages":"Article 107490"},"PeriodicalIF":9.1,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Antibiotic resistance is a global health concern that is rapidly spreading among human and animal pathogens. Developing novel antibiotics is one of the most significant approaches to surmount antibiotic resistance. Given the difficult in identifying novel targets, cryptic binding sites provide new pockets for compounds design to combat antibiotic resistance. However, there exists a lack of comprehensive analysis and discussion on the successful utilization of cryptic pockets in overcoming antibiotic resistance. Here, we systematically analyze the crucial role of cryptic pockets in neutralizing antibiotic resistance. First, antibiotic resistance development and associated resistance mechanisms are summarized. Then, the advantages and mechanisms of cryptic pockets for overcoming antibiotic resistance were discussed. Specific cryptic pockets in resistant proteins and successful case studies of designed inhibitors are exemplified. This review provides insight into the discovery of cryptic pockets for drug design as an approach to overcome antibiotic resistance
{"title":"New avenues of combating antibiotic resistance by targeting cryptic pockets","authors":"Yangyang Gao , Huimin Chen , Weicheng Yang , Shuang Wang , Daohong Gong , Xiao Zhang , Yuanqin Huang , Vinit Kumar , Qiuqian Huang , W.M.W.W. Kandegama , Gefei Hao","doi":"10.1016/j.phrs.2024.107495","DOIUrl":"10.1016/j.phrs.2024.107495","url":null,"abstract":"<div><div>Antibiotic resistance is a global health concern that is rapidly spreading among human and animal pathogens. Developing novel antibiotics is one of the most significant approaches to surmount antibiotic resistance. Given the difficult in identifying novel targets, cryptic binding sites provide new pockets for compounds design to combat antibiotic resistance. However, there exists a lack of comprehensive analysis and discussion on the successful utilization of cryptic pockets in overcoming antibiotic resistance. Here, we systematically analyze the crucial role of cryptic pockets in neutralizing antibiotic resistance. First, antibiotic resistance development and associated resistance mechanisms are summarized. Then, the advantages and mechanisms of cryptic pockets for overcoming antibiotic resistance were discussed. Specific cryptic pockets in resistant proteins and successful case studies of designed inhibitors are exemplified. This review provides insight into the discovery of cryptic pockets for drug design as an approach to overcome antibiotic resistance</div></div>","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"210 ","pages":"Article 107495"},"PeriodicalIF":9.1,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-02DOI: 10.1016/j.phrs.2024.107491
Valentina Tedeschi , Valeria Nele , Valeria Valsecchi , Serenella Anzilotti , Antonio Vinciguerra , Laura Zuccaro , Maria Josè Sisalli , Chiara Cassiano , Nunzia De Iesu , Giuseppe Pignataro , Lorella Maria Teresa Canzoniero , Anna Pannaccione , Giuseppe De Rosa , Agnese Secondo
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease currently incurable, in which motor neuron degeneration leads to voluntary skeletal muscle atrophy. Molecularly, ALS is characterized by protein aggregation, synaptic and organellar dysfunction, and Ca2+ dyshomeostasis. Of interest, autophagy dysfunction is emerging as one of the main putative targets of ALS therapy. A tune regulation of this cleansing process is affordable by a proper stimulation of TRPML1, one of the main lysosomal channels. However, TRPML1 activation by PI(3,5)P2 has low open probability to remain in an active conformation. To overcome this drawback we developed a lipid-based formulation of PI(3,5)P2 whose putative therapeutic potential has been tested in in vitro and in vivo ALS models.
Pharmacodynamic properties of PI(3,5)P2 lipid-based formulations (F1 and F2) on TRPML1 activity have been characterized by means of patch-clamp electrophysiology and Fura-2AM video-imaging in motor neuronal cells. Once selected for the ability to stabilize TRPML1 activity, the most effective preparation F1 was studied in vivo to measure neuromuscular function and survival of SOD1G93A ALS mice, thereby establishing its therapeutic profile.
F1, but not PI(3,5)P2 alone, stabilized the open state of the lysosomal channel TRPML1 and increased the persistence of intracellular calcium concentration ([Ca2+]i). Then, F1 was effective in delaying motor neuron loss, improving innervated endplants and muscle performance in SOD1G93A mice, extending overall lifespan by an average of 10 days. Of note F1 prevented gliosis and autophagy dysfunction in ALS mice by restoring PI(3,5)P2 level.
Our novel self-assembling lipidic formulation for PI(3,5)P2 delivery exerts a neuroprotective effect in preclinical models of ALS mainly regulating dysfunctional autophagy through TRPML1 activity stabilization.
背景和目的：肌萎缩性脊髓侧索硬化症（ALS）是一种进行性神经退行性疾病，目前无法治愈，运动神经元变性会导致自主性骨骼肌萎缩。从分子角度看，肌萎缩侧索硬化症的特征是蛋白质聚集、突触和细胞器功能障碍以及 Ca2+ 平衡失调。值得关注的是，自噬功能障碍正在成为 ALS 治疗的主要假定靶点之一。通过适当刺激主要溶酶体通道之一的 TRPML1，可以对这一清洁过程进行调节。然而，PI(3,5)P2 激活的 TRPML1 保持活性构象的开放概率较低。为了克服这一缺点，我们开发了一种基于脂质的 PI(3,5)P2 制剂，其治疗潜力已在体外和体内 ALS 模型中进行了测试：实验方法：通过运动神经细胞中的贴片钳电生理学和 Fura-2AM 视频成像，确定了 PI(3,5)P2 脂基制剂（F1 和 F2）对 TRPML1 活性的药效学特性。在筛选出能稳定 TRPML1 活性的制剂后，对最有效的制剂 F1 进行了体内研究，以测量 SOD1G93A ALS 小鼠的神经肌肉功能和存活率，从而确定其治疗特性。主要结果 F1（而不是单独的 PI(3,5)P2）稳定了溶酶体通道 TRPML1 的开放状态，并增加了细胞内钙浓度（[Ca2+]i）的持续性。然后，F1 能有效延缓 SOD1G93A 小鼠运动神经元的丧失，改善神经支配内植物和肌肉性能，平均延长整体寿命 10 天。值得注意的是，F1通过恢复PI(3,5)P2水平，防止了ALS小鼠的神经胶质增生和自噬功能障碍：我们用于递送 PI(3,5)P2 的新型自组装脂质制剂在 ALS 临床前模型中发挥了神经保护作用，主要是通过稳定 TRPML1 的活性来调节自噬功能障碍。
{"title":"Nanoparticles encapsulating phosphatidylinositol derivatives promote neuroprotection and functional improvement in preclinical models of ALS via a long-lasting activation of TRPML1 lysosomal channel","authors":"Valentina Tedeschi , Valeria Nele , Valeria Valsecchi , Serenella Anzilotti , Antonio Vinciguerra , Laura Zuccaro , Maria Josè Sisalli , Chiara Cassiano , Nunzia De Iesu , Giuseppe Pignataro , Lorella Maria Teresa Canzoniero , Anna Pannaccione , Giuseppe De Rosa , Agnese Secondo","doi":"10.1016/j.phrs.2024.107491","DOIUrl":"10.1016/j.phrs.2024.107491","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease currently incurable, in which motor neuron degeneration leads to voluntary skeletal muscle atrophy. Molecularly, ALS is characterized by protein aggregation, synaptic and organellar dysfunction, and Ca<sup>2+</sup> dyshomeostasis. Of interest, autophagy dysfunction is emerging as one of the main putative targets of ALS therapy. A tune regulation of this cleansing process is affordable by a proper stimulation of TRPML1, one of the main lysosomal channels. However, TRPML1 activation by PI(3,5)P<sub>2</sub> has low open probability to remain in an active conformation. To overcome this drawback we developed a lipid-based formulation of PI(3,5)P<sub>2</sub> whose putative therapeutic potential has been tested in <em>in vitro</em> and <em>in vivo</em> ALS models.</div><div>Pharmacodynamic properties of PI(3,5)P<sub>2</sub> lipid-based formulations (F1 and F2) on TRPML1 activity have been characterized by means of patch-clamp electrophysiology and Fura-2AM video-imaging in motor neuronal cells. Once selected for the ability to stabilize TRPML1 activity, the most effective preparation F1 was studied <em>in vivo</em> to measure neuromuscular function and survival of SOD1<sup>G93A</sup> ALS mice, thereby establishing its therapeutic profile.</div><div>F1, but not PI(3,5)P<sub>2</sub> alone<sub>,</sub> stabilized the open state of the lysosomal channel TRPML1 and increased the persistence of intracellular calcium concentration ([Ca<sup>2+</sup>]<sub>i</sub>). Then, F1 was effective in delaying motor neuron loss, improving innervated endplants and muscle performance in SOD1<sup>G93A</sup> mice, extending overall lifespan by an average of 10 days. Of note F1 prevented gliosis and autophagy dysfunction in ALS mice by restoring PI(3,5)P<sub>2</sub> level.</div><div>Our novel self-assembling lipidic formulation for PI(3,5)P<sub>2</sub> delivery exerts a neuroprotective effect in preclinical models of ALS mainly regulating dysfunctional autophagy through TRPML1 activity stabilization.</div></div>","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"210 ","pages":"Article 107491"},"PeriodicalIF":9.1,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-02DOI: 10.1016/j.phrs.2024.107492
Yi Shan , Jiayu Lu , Hua Qian , Zhaomin Xia , Xiaoxue Mo , Meidi An , Wen Yang , Siqi Wang , Delu Che , Cheng Wang , Huaizhen He
Traditional Chinese medicine (TCM) contributes significantly to human health. Owing to the complexity of the ingredients in TCM, it is necessary to conduct basic research on effective substances and identify toxic substances to control the safety of medication. Cell membrane chromatography (CMC) is an important method for identifying target components in complex systems. The cell membrane stationary phase (CMSP) is the core component and key factor in determining the effectiveness of CMC. This review summarizes the development of CMSP with different membrane protein immobilization strategies and the application of CMC in the discovery of active and toxic substances in TCM, with the aim of providing an effective means for the discovery of active ingredients and quality control of TCM.
{"title":"Immobilized protein strategies based on cell membrane chromatography and its application in discovering active and toxic substances in traditional Chinese medicine","authors":"Yi Shan , Jiayu Lu , Hua Qian , Zhaomin Xia , Xiaoxue Mo , Meidi An , Wen Yang , Siqi Wang , Delu Che , Cheng Wang , Huaizhen He","doi":"10.1016/j.phrs.2024.107492","DOIUrl":"10.1016/j.phrs.2024.107492","url":null,"abstract":"<div><div>Traditional Chinese medicine (TCM) contributes significantly to human health. Owing to the complexity of the ingredients in TCM, it is necessary to conduct basic research on effective substances and identify toxic substances to control the safety of medication. Cell membrane chromatography (CMC) is an important method for identifying target components in complex systems. The cell membrane stationary phase (CMSP) is the core component and key factor in determining the effectiveness of CMC. This review summarizes the development of CMSP with different membrane protein immobilization strategies and the application of CMC in the discovery of active and toxic substances in TCM, with the aim of providing an effective means for the discovery of active ingredients and quality control of TCM.</div></div>","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"210 ","pages":"Article 107492"},"PeriodicalIF":9.1,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-02DOI: 10.1016/j.phrs.2024.107493
Yunxia Li , Qi Han , Yuxin Liu , Jie Yin , Jie Ma
Lipids play crucial roles in signal transduction. Lipid metabolism is associated with several transcriptional regulators, including peroxisome proliferator activated receptor γ, sterol regulatory element-binding protein 1, and acetyl-CoA carboxylase. In recent years, increasing evidence has suggested that members of the histone deacetylase (HDAC) family play key roles in lipid metabolism. However, the mechanisms by which each member of this family regulates lipid metabolism remain unclear. This review discusses the latest research on the roles played by HDACs in fat metabolism. The role of HDACs in obesity, diabetes, and atherosclerosis has also been discussed. In addition, the interaction of HDACs with the gut microbiome and circadian rhythm has been reviewed, and the future development trend in HDACs has been predicted, which may potentiate therapeutic application of targeted HDACs in related metabolic diseases.
{"title":"Role of the histone deacetylase family in lipid metabolism: Structural specificity and functional diversity","authors":"Yunxia Li , Qi Han , Yuxin Liu , Jie Yin , Jie Ma","doi":"10.1016/j.phrs.2024.107493","DOIUrl":"10.1016/j.phrs.2024.107493","url":null,"abstract":"<div><div>Lipids play crucial roles in signal transduction. Lipid metabolism is associated with several transcriptional regulators, including peroxisome proliferator activated receptor γ, sterol regulatory element-binding protein 1, and acetyl-CoA carboxylase. In recent years, increasing evidence has suggested that members of the histone deacetylase (HDAC) family play key roles in lipid metabolism. However, the mechanisms by which each member of this family regulates lipid metabolism remain unclear. This review discusses the latest research on the roles played by HDACs in fat metabolism. The role of HDACs in obesity, diabetes, and atherosclerosis has also been discussed. In addition, the interaction of HDACs with the gut microbiome and circadian rhythm has been reviewed, and the future development trend in HDACs has been predicted, which may potentiate therapeutic application of targeted HDACs in related metabolic diseases.</div></div>","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"210 ","pages":"Article 107493"},"PeriodicalIF":9.1,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.phrs.2024.107329
Kaiqing Li, Xue Xia, Tong Fu, Ying Tong
{"title":"Commentary on “Apabetalone, a BET protein inhibitor, inhibits kidney damage in diabetes by preventing pyroptosis via modulating the P300/H3K27ac/PLK1 axis”","authors":"Kaiqing Li, Xue Xia, Tong Fu, Ying Tong","doi":"10.1016/j.phrs.2024.107329","DOIUrl":"10.1016/j.phrs.2024.107329","url":null,"abstract":"","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"209 ","pages":"Article 107329"},"PeriodicalIF":9.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.phrs.2024.107455
Guido Grassi , Giuseppe Mancia
{"title":"Editorial – New European ESH and ESC guidelines for the management of hypertension: More similarities than differences","authors":"Guido Grassi , Giuseppe Mancia","doi":"10.1016/j.phrs.2024.107455","DOIUrl":"10.1016/j.phrs.2024.107455","url":null,"abstract":"","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"209 ","pages":"Article 107455"},"PeriodicalIF":9.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.phrs.2024.107463
Delong Chen , Zhen Ye , Chao Wang , Qingqing Wang , Haibin Wang , Vincent Kuek , Ziyi Wang , Heng Qiu , Jinbo Yuan , Jacob Kenny , Fan Yang , Jianbo He , Yun Liu , Gang Wang , Meng Zhang , Gangyu Zhang , Junjian Wang , Peng Chen , Jiake Xu
{"title":"Corrigendum to “Arctiin abrogates osteoclastogenesis and bone resorption via suppressing RANKL-induced ROS and NFATc1 activation” [Pharmacol. Res. 159 (2020) 104944]","authors":"Delong Chen , Zhen Ye , Chao Wang , Qingqing Wang , Haibin Wang , Vincent Kuek , Ziyi Wang , Heng Qiu , Jinbo Yuan , Jacob Kenny , Fan Yang , Jianbo He , Yun Liu , Gang Wang , Meng Zhang , Gangyu Zhang , Junjian Wang , Peng Chen , Jiake Xu","doi":"10.1016/j.phrs.2024.107463","DOIUrl":"10.1016/j.phrs.2024.107463","url":null,"abstract":"","PeriodicalId":19918,"journal":{"name":"Pharmacological research","volume":"209 ","pages":"Article 107463"},"PeriodicalIF":9.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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